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Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells

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Title: Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells
Authors: Kameoka, Shoichiro Browse this author
Kameyama, Takeshi Browse this author →KAKEN DB
Hayashi, Takaya Browse this author
Sato, Seiichi Browse this author
Ohnishi, Naomi Browse this author
Hayashi, Takeru Browse this author
Murata-Kamiya, Naoko Browse this author
Higashi, Hideaki Browse this author →KAKEN DB
Hatakeyama, Masanori Browse this author →KAKEN DB
Takaoka, Akinori Browse this author →KAKEN DB
Issue Date: Feb-2016
Publisher: Biomedical Research Press
Journal Title: Biomedical Research
Volume: 37
Issue: 1
Start Page: 21
End Page: 27
Publisher DOI: 10.2220/biomedres.37.21
PMID: 26912137
Abstract: More than 50% of people in the world are infected with Helicobacter pylori (H. pylori), which induces various gastric diseases. Especially, epidemiological studies have shown that H. pylori infection is a major risk factor for gastric cancer. It has been reported that the levels of interleukin (IL)-1β are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1β during H. pylori infection. We found that IL-1βmRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1β production was inhibited by a caspase-1 inhibitor and a ROS inhibitor. Furthermore, K+ efflux and Ca2+ signaling were also involved in this process. These data suggest that NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) and its complex, known as NLRP3 inflammasome, are involved in IL-1β production during H. pylori infection because it is reported that NLRP3 inflammasome is activated by ROS, K+ efflux and/or Ca2+ signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients.
Type: article
URI: http://hdl.handle.net/2115/61351
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 高岡 晃教

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